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Clinical aspects of radiation injury.pptx

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RADIATION LEUKO.pptx
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Clinical aspects of radiation injury.pptx

  1. 1.  The less mature cells are more radiosensitive than the more mature cells  So cell in active mitosis like the stem cells are more affected than cells that divide slowly like neurons
  2. 2.  However later experiments on flies have shown the ionizing radiation is capable of mutation induction which can be similar to some extent to spontaneous mutation in nature  The effects of these radiation depends on the total dose and the duration of exposure
  3. 3.  Injury following radiation exposure may be not specific as can occur due to chemical or heat exposure  There is a period of latency for observable response to happen that may range from decades for low radiation doses to minutes of hours for larger doses
  4. 4. Direct interaction Indirect interaction
  5. 5.  The cell’s macromolecules as proteins and DNA are hit by ionizing radiation and they are either killed or mutated  It is hard to permanently destroy or break double stranded DNA than single stranded DNA  However certain cells react as if they contain single stranded DNA so being more radiosensitive
  6. 6.  It the hit causes complete break or permanent damage of DNA these cells die or eventually die  However humans have abundance of cellular repair process that can replace the died ones  Only when this replacement mechanism falters , the radiation effects are seen which occurs probably at higher doses of radiation
  7. 7.  Actively dividing cells are more sensitive  Among the 4 stages of cell division the M phase when the chromosomes are condensed and paired is the most radiosensitive  Cancer cells being more dividing and having more chromatin in them are considered more radiosensitive than the normal cells
  8. 8.  This occurs when the radiation injury is deposited in the cells  The interaction here occurs with the cellular water not with the macromolecules  Hydrolysis of water ultimately results in the formation of hydrogen peroxide which further affects many cellular processes inside the cells  Here comes the role of antioxidants as anticancer agents
  9. 9. Division delay Reproductive failure Interphase death
  10. 10.  Dose dependent pattern with doses from 0.5 Gray to 3 Gy  After a period of delay it returns back to near normal for unknown reasons  However above the dose of 3 Gy the mitotic rate may not recover the division may never happen
  11. 11.  It is also dose dependent  At doses below 1.5 Gy it occurs in random non linear pattern  However above 1.5 Gy it is non random and linear
  12. 12.  Cell death can occur many generations from the initial radiation exposure  It is thought it can be due to apoptosis or arrest of cell replication  Immature rapidly dividing cells are more sensitive
  13. 13. As a general role, any type of cell injury as a result of direct or indirect interaction with ionizing radiation
  14. 14. Linear threshold Linear no threshold Linear quadratic
  15. 15. Stochastic Non stochastic
  16. 16. Acute effects Chronic effects
  17. 17.  Ionizing radiation are considered harmless at the diagnostic or background level  Above the dose of 0.5 Gy effects start at a linear fashion and in non stochastic pattern  Some chromosome aberrations may be seen at doses below 0.5 Gy but with no clinical symptoms
  18. 18.  They are primarily stochastic  Cancer is the primary concern  However non cancerous effects like cataract may also occur  Leukemia may occur as one of stochastic effects of radiation with doses of 50-100 rads  At doses of 100-500 rads there is a linear relation with leukemia
  19. 19.  Data suggest that the rate of leukemia incidence by 1-2 cases per million with every rad of exposure  There is a latency of 14 years  Higher doses are associated with other types of cancer like lung, bone, thyroid etc
  20. 20.  Depletion of BM and peripheral blood cells together with loss of lymphoid organs weight are well established side effects  MSCs seem more radioresistant than the HPSCs  This may be attributed to oxidative stress resistance
  21. 21.  This observation was confirmed with the finding in transplanted patients received TBI showing the MSCs are the host’s not the donor’s indicating radio- resistance  MSCs also retain their differentiation ability shown by the increased adipocytes in BM of murine models achieving bone marrow failure
  22. 22.  This preferential differentiation towards adipocytes comes at the expense of osteoblasts explaining osteoporosis and altered bone marrow micorenvironment following irradiation exposure

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